Centrosomes at M phase act as a scaffold for the accumulation of intracellular ubiquitinated proteins

Kimura, Hiroyuki; Miki, Yoshio; Nakanishi, Akira

doi:10.4161/cc.28896

Cited by 12 publications

(10 citation statements)

References 38 publications

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“…A recent analysis using microarrayed Tyr(P) peptides representing confirmed and theoretical phosphorylation motifs from the cellular proteome, identifies more than 130 potential CDC25B substrates ( Zhao et al, 2015 ). These substrates are implicated in microtubule dynamics, signalling pathways like Delta/Notch or Wnt, transcription, epigenetic modifications, mitotic spindle or proteasome activity ( Zhao et al, 2015 ), and several of them could play a role in INM or cell fate choice ( Akhtar et al, 2009 ; Aubert et al, 2002 ; Das and Storey, 2012 ; Götz and Huttner, 2005 ; Hämmerle and Tejedor, 2007 ; Jiang and Hsieh, 2014 ; Kimura et al, 2014 ; Li et al, 2012 ; MuhChyi et al, 2013 ; Olivera-Martinez et al, 2014 ; Sato et al, 2004 ; Schwartz and Pirrotta, 2007 ; Vilas-Boas et al, 2011 ). Further work will be necessary to dissect the molecular pathway linking CDC25B with INM and to determine whether this link is causal in neurogenesis.…”

Section: Discussionmentioning

confidence: 99%

Neurogenic decisions require a cell cycle independent function of the CDC25B phosphatase

Bonnet

Molina

Roussat

et al. 2018

eLife

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A fundamental issue in developmental biology and in organ homeostasis is understanding the molecular mechanisms governing the balance between stem cell maintenance and differentiation into a specific lineage. Accumulating data suggest that cell cycle dynamics play a major role in the regulation of this balance. Here we show that the G2/M cell cycle regulator CDC25B phosphatase is required in mammals to finely tune neuronal production in the neural tube. We show that in chick neural progenitors, CDC25B activity favors fast nuclei departure from the apical surface in early G1, stimulates neurogenic divisions and promotes neuronal differentiation. We design a mathematical model showing that within a limited period of time, cell cycle length modifications cannot account for changes in the ratio of the mode of division. Using a CDC25B point mutation that cannot interact with CDK, we show that part of CDC25B activity is independent of its action on the cell cycle.

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Section: Discussionmentioning

confidence: 99%

Neurogenic decisions require a cell cycle independent function of the CDC25B phosphatase

Bonnet

Molina

Roussat

et al. 2018

eLife

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“…Depletion of the endogenous proteasome inhibitor Ecm29 86 led to a significant reduction in polyubiquitinated proteins at the centrosome, supporting the view that these substrates may be actively degraded by centrosomal proteasomes. 87 While proteasomal activity is roughly the same between S-phase and M-phase centrosomes, centrosomal targeting of polyubiquitinated proteins increases during maturation, demonstrating that other substrates may share this mode of division-coupled regulation. Together, these studies suggest that centrosome-associated degradation strategies control various signaling factors during mitotic divisions, linking pathway activity to the cell cycle.…”

Section: Centrosome-associated Degradation Of Cell Fate Determinantsmentioning

confidence: 99%

The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation

Vora

Phillips

2016

Cell Cycle

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The centrosome is the major microtubule-organizing center in animal cells but is dispensable for proper microtubule spindle formation in many biological contexts and is thus thought to fulfill additional functions. Recent observations suggest that the centrosome acts as a scaffold for proteasomal degradation in the cell to regulate a variety of biological processes including cell fate acquisition, cell cycle control, stress response, and cell morphogenesis. Here, we review the body of studies indicating a role for the centrosome in promoting proteasomal degradation of ubiquitin-proteasome substrates and explore the functional relevance of this system in different biological contexts. We discuss a potential role for the centrosome in coordinating local degradation of proteasomal substrates, allowing cells to achieve stringent spatiotemporal control over various signaling processes.

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“…A recent analysis using microarrayed Tyr(P) peptides representing confirmed and theoretical phosphorylation motifs from the cellular proteome, identifies more than 130 potential CDC25B substrates (Zhao et al, 2015). These substrates are implicated in signalling pathways like Delta/Notch or Wnt, in microtubule dynamics, transcription, epigenetic modifications, mitotic spindle or proteasome activity (Zhao et al, 2015), and all of them could play role in cell fate choice (Akhtar et al, 2009; Aubert, Dunstan, Chambers, & Smith, 2002; Das & Storey, 2012; Gotz & Huttner, 2005; Hammerle & Tejedor, 2007; Jiang & Hsieh, 2014; Kimura, Miki, & Nakanishi, 2014; Li et al, 2012; MuhChyi, Juliandi, Matsuda, & Nakashima, 2013; Olivera-Martinez et al, 2014; Sato, Meijer, Skaltsounis, Greengard, & Brivanlou, 2004; Schwartz & Pirrotta, 2007; Vilas-Boas, Fior, Swedlow, Storey, & Henrique, 2011).…”

Section: Discussionmentioning

confidence: 99%

Neurogenic decisions require a cell cycle independent function of the CD25B phosphatase

Bonnet

Roussat

Molina

et al. 2017

Preprint

View full text Add to dashboard Cite

A fundamental issue in developmental biology and in organ homeostasis is understanding the molecular mechanisms governing the balance between stem cell maintenance and differentiation into a specific lineage. Accumulating data suggest that cell cycle dynamics plays a major role in the regulation of this balance. Here we show that the G2/M cell cycle regulator CDC25B phosphatase is required in mammals to finely tune neuronal production in the neural tube. We show that in chick neural progenitors, CDC25B activity is both required and sufficient to stimulate neurogenic divisions and to promote neuronal differentiation. We design a mathematical model showing that within a limited period of time, cell cycle length modifications cannot account for changes in the ratio of the mode of division. Using a CDC25B point mutation that cannot interact with CDK, we show that part of CDC25B activity on neurogenic divisions is independent of its action on the cell cycle.

show abstract

Centrosomes at M phase act as a scaffold for the accumulation of intracellular ubiquitinated proteins

Cited by 12 publications

References 38 publications

Neurogenic decisions require a cell cycle independent function of the CDC25B phosphatase

Neurogenic decisions require a cell cycle independent function of the CDC25B phosphatase

The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation

Neurogenic decisions require a cell cycle independent function of the CD25B phosphatase

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